Particulate Air Pollutants and Airway Inflammation

Abstract

Particulate air pollutants emanating from traffic and various industries are related to allergic airway disorders including asthma. Particulate air pollutants inhalation directly induces lung inflammation to allergens or respiratory viral infection as an adjuvant by macrophages and epithelial cells. Inhalation of particulate air pollutants aggravates respiratory symptoms in patients with chronic airway diseases, but the mechanisms underlying this response remain poorly understood. Diesel exhaust particles induced airway hyperresponsiveness and Ym mRNA expression via a Th2 cell-biased response, which synthesized by activated macrophages are homologous to chitinase and have chitinase activity. Alveolar macrophages play an important role in particles-induced airway and lung inflammation via direct production of IL-13. Treatment of epithelial cells with bovine serum albumin coated titanium dioxide particles altered 20 protein spots on the two-dimensional gel, and these were then analyzed by nano-LC-MS/MS. These proteins included defense-related, cell-activating, and cytoskeletal proteins implicated in the response to oxidative stress. TiO2 treatment was found to increase the amount of mRNA for macrophage migration-inhibitory factor (MIF). MIF was expressed primarily in epithelium and was elevated in lung tissues and bronchoalveolar lavage fluids of TiO2-treated rats as compared with sham treated rats. Carbon black and diesel exhaust particles also induced expression of MIF protein in the epithelial cells. We attempt to offer insight into how particles may influence airway inflammation.